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Updated: Oct 23, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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Epigenetic control of melanoma cell invasiveness by the stem cell factor SALL4

Johanna Diener1, Arianna Baggiolini1,2, Mattias Pernebrink3,4

  • 1University of Zürich, Institute of Anatomy, Zürich, Switzerland.

Nature Communications
|August 21, 2021
PubMed

Insights

Embryonic stem cell factor Sall4 is crucial for melanoma formation. Its loss prevents primary tumors but surprisingly promotes distant micrometastases by inducing a switch to an invasive phenotype.

Area of Science:

  • Oncology
  • Developmental Biology
  • Molecular Biology

Background:

  • Melanoma progression involves reactivation of developmental programs.
  • Embryonic stem cell (ESC) factor Sall4 is implicated in tumor initiation.

Purpose of the Study:

  • To investigate the role of Sall4 in melanoma initiation and progression.
  • To elucidate the mechanism by which Sall4 influences melanoma invasiveness.

Main Methods:

  • Utilized a Tyr::NrasQ61K; Cdkn2a-/- melanoma mouse model.
  • Performed transcriptional profiling and in vitro assays on human melanoma cells.
  • Investigated the interaction between Sall4 and histone deacetylase 2 (HDAC2).

Main Results:

  • Sall4 re-expression was observed in melanoma.
  • Sall4 loss prevented primary melanoma formation but promoted distant micrometastases.
  • Sall4 knockdown induced a phenotype switch towards invasiveness in melanoma cells.
  • Sall4 negatively regulates invasiveness via interaction with HDAC2 and co-binding to invasiveness genes.

Conclusions:

  • Sall4 plays a critical role in regulating melanoma phenotype switching.
  • Sall4 controls melanoma invasiveness through an HDAC2-mediated mechanism.
  • Targeting Sall4 or HDAC activity may offer therapeutic strategies for melanoma metastasis.

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